The loss of functional myocardium subsequent to acute myocardial infarction remains an important cause for the development of morbidity and mortality. Great efforts have been devoted to the development of surgical and/or pharmacologic means of preserving ischemic myocardium in an effort to prevent deterioration of cardiac function. Thus, therapy designed to minimize the destruction of ischemic myocardium should be beneficial in maintaining pump function and perhaps, preventing serious disturbances in cardiac rhythm, especially in the early stages of acute ischemic episodes or during reperfusion of the ischemic myocardium. One objective of this proposal will be to determine if pharmacologic interventions can prevent or reduce the hazards associated with reperfusion of the regionally ischemic myocardium. A new class of pharmacologic agents, quaternary ammonium compounds, will be examined for their potential to protect the ischemic heart in the experimental animal. The agents to be tested are related structurally to propranolol, but unlike the latter compound, they do not produce beta-receptor blockade. Like propranolol, however, they are capable of decreasing myocardial oxygen consumption and theoretically should be able to protect the ischemic myocardial cell from irreversible cellular damage. This proposal outlines a series of studies designed to test these and related drugs in several different experimental models that mimic clinical conditions associated with ischemic myocardial damage.